Background: Epidemiologic associations of leukocyte telomere length (LTL) and pancreatic ductal adenocarcinoma (PDAC) have been inconsistent owing, in part, to variation in telomere length (TL) assessment across studies. To overcome this limitation and address concerns of potential reverse causation, we used carriage of telomere-related alleles to genetically predict TL and examined its association with PDAC.

Methods: A case–control study of 1,500 PDAC cases and 1,500 controls, frequency-matched on age and sex was performed. Eight of nine polymorphisms previously associated with variation in LTL were analyzed. Genetic risk scores (GRS) consisting of the TL-related polymorphisms were computed as the number of long TL alleles carried by an individual scaled to published kilobase pairs of TL associated with each allele. Participants were further categorized on the basis of the number of short TL alleles they carry across all eight SNPs. Associations were examined in additive and dominant models using logistic regression to calculate ORs and 95% confidence intervals (CI).

Results: In age- and sex-adjusted models, one short TL allele (rs10936599, T) was associated with reduced risk, whereas another short TL allele (rs2736100, A) was associated with increased risk, with per-allele ORs of 0.89 (95% CI, 0.79–0.99) and 1.13 (95% CI, 1.01–1.24), respectively. No association was observed with GRS or short TL allele counts, and no associations were observed in the dominant models.

Conclusions: Findings suggest that genetically predicted short TL is not associated with PDAC risk.

Impact: Common genetic determinants of short TL do not appear to influence PDAC risk. Cancer Epidemiol Biomarkers Prev; 26(6); 971–4. ©2017 AACR.

Telomere length (TL), the repetitive DNA sequence (TTAGGG) that spans the ends of linear chromosomes, protect genetic material from degradation, prevent end-to-end fusion, and ensure proper chromosomal segregation (1). Individual variation in TL can result from differences in demographic, lifestyle, and genetic factors. Blackburn and colleagues estimated that as much as 80% of interindividual variation in TL is attributable to genetic factors (1). Epidemiologic studies have reported conflicting results for association between leukocyte TL (LTL) and pancreatic ductal adenocarcinoma (PDAC; reviewed in ref. 2). Long LTL was associated with increased PDAC risk in one prospective study, but reduced risk in another, and a “U-shaped” association was reported by one case–control and one prospective study (2). In light of the conflicting findings, we genotyped nine SNPs that have been associated with variation in LTL to genetically predict TL and examined its association with PDAC.

Following approval by the Mayo Clinic Institutional Review Board, epidemiologic data and leukocyte DNA were obtained from the Mayo Clinic pancreatic cancer patient registry. The registry utilizes an ultra-rapid case ascertainment process for prospective patient recruitment. Previously enrolled noncancer control patients by the registry were frequency-matched to incident PDAC cases on age and sex. The study included 1,500 cases and 1,500 controls enrolled between October 2000 and June 2016. Participants completed identical risk factor questionnaires that solicited various information including demographics, smoking history, personal history of diabetes, and usual adult weight and height.

Genotyping of the leukocyte DNA was performed by the Mayo Clinic Genome Analysis Core. Nine SNPs previously associated with variation in LTL (Table 1) were genotyped using the Sequenom multiplex assay. Genotyping call rates and concordance with blinded duplicates were 100% each. Hardy–Weinberg equilibrium among controls was violated for one SNP (rs755017; P value < 0.05). This SNP was eliminated from further analyses. One control sample failed genotyping, leaving 1,500 cases and 1,499 controls for analyses.

Table 1.

Polymorphic variants associated with leukocyte TL in genome-wide association studies, and minor allele frequencies in the current study

SNP IDPosition (GRCh37/hg19)Nearby geneShort alleleLong alleleaMAFPublished βbPublished PReference articlesMAF Controlsc
rs10936599 chr3:169492101 TERC T C 0.25 0.117 2.5 × 10−31 Codd et al. (6) 0.261 
rs2736100 chr5:1286516 TERT A C 0.49 0.094 4.4 × 10−19 Codd et al. (6) 0.492 
rs7675998 chr4:164007820 NAF1 A G 0.22 0.090 4.3 × 10−16 Codd et al. (6) 0.210 
rs9420907 chr10:105676465 OBFC1 A C 0.14 0.083 6.9 × 10−11 Codd et al. (6) 0.143 
rs6772228 chr3:58376019 PXK A T 0.05 0.120 3.9 × 10−10 Pooley et al. (7) 0.048 
rs8105767 chr19:22215441 ZNF208 A G 0.30 0.058 1.1 × 10−9 Codd et al. (6) 0.295 
rs755017* chr20:62421622 RTEL1 A G 0.12 0.074 6.7 × 10−9 Codd et al. (6) 0.004 
rs11125529 chr2:54475866 ACYP2 C A 0.14 0.067 4.5 × 10−8 Codd et al. (6) 0.140 
rs3027234 chr17:8136092 CTC1 T C 0.23 0.057 2.3 × 10−8 Mangino et al. (8) 0.231 
SNP IDPosition (GRCh37/hg19)Nearby geneShort alleleLong alleleaMAFPublished βbPublished PReference articlesMAF Controlsc
rs10936599 chr3:169492101 TERC T C 0.25 0.117 2.5 × 10−31 Codd et al. (6) 0.261 
rs2736100 chr5:1286516 TERT A C 0.49 0.094 4.4 × 10−19 Codd et al. (6) 0.492 
rs7675998 chr4:164007820 NAF1 A G 0.22 0.090 4.3 × 10−16 Codd et al. (6) 0.210 
rs9420907 chr10:105676465 OBFC1 A C 0.14 0.083 6.9 × 10−11 Codd et al. (6) 0.143 
rs6772228 chr3:58376019 PXK A T 0.05 0.120 3.9 × 10−10 Pooley et al. (7) 0.048 
rs8105767 chr19:22215441 ZNF208 A G 0.30 0.058 1.1 × 10−9 Codd et al. (6) 0.295 
rs755017* chr20:62421622 RTEL1 A G 0.12 0.074 6.7 × 10−9 Codd et al. (6) 0.004 
rs11125529 chr2:54475866 ACYP2 C A 0.14 0.067 4.5 × 10−8 Codd et al. (6) 0.140 
rs3027234 chr17:8136092 CTC1 T C 0.23 0.057 2.3 × 10−8 Mangino et al. (8) 0.231 

Abbreviation: MAF, minor allele frequency (among controls).

aAllele associated with longer leukocytes telomere length.

bβ-estimate is reported in kilobase pairs per long telomere length allele.

cMAF, minor allele frequencies among controls in the current study (n = 1,499).

*This polymorphism was not in Hardy–Weinberg equilibrium (P < 0.05) and was excluded from the analysis.

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Per-allele ORs and 95% confidence intervals (CI) were calculated with logistic regression, using alleles previously associated with long LTL as the referent alleles. Genetic risk scores (GRS) were computed by combining data on all eight TL-related SNPs and calculated according to published β-estimates of kilobase pairs of LTL associated with each allele, as described previously (3). The GRS were categorized into quartiles (on the basis of control distribution), using the lowest quartile as the referent group. Participants were further categorized according to the number of short TL-associated alleles they carry. We explored associations of LTL-related SNPs and short TL allele counts in dominant models: participants with one or two copies of the short TL allele were combined into one group and compared with those who carry two copies of the long TL allele. Analyses were performed in SAS (v9.4).

Compliance with ethical standards

Written informed consent was obtained from all participants. The study was approved by the Mayo Clinic Institutional Review Board.

By design, the cases and controls were similar in age and sex (Supplementary Table S1). There were greater proportion of current smokers, individuals with personal history of diabetes, and a slightly higher body mass index (BMI) among cases than controls (28 vs. 27 kg/m2). After adjusting for age and sex, the short TL-associated allele of rs10936599 was associated with lower PDAC risk [OR, 0.89; 95% confidence interval (CI), 0.79–0.99], whereas the short TL-associated allele of rs2736100 was associated with higher risk (OR, 1.13, 95%CI, 1.02–1.24; Table 2A). None of these associations remained significant after additional adjustment for diabetes, smoking, and BMI. No associations were observed with GRS or short TL allele counts. Similarly, no associations were observed in the dominant models (Table 2B).

Table 2A.

Associations of telomere-related SNPs, genetic risk scores, and short TL allele counts with pancreatic ductal adenocarcinoma risk: additive model (cases: n, 1,500; controls: n, 1,499)

Unadjusted modelAge- and sex-adjustedMultivariable-adjusteda
SNP IDMAFOR (95% CI)POR (95% CI)POR (95% CI)P
rs10936599 0.261 0.89 (0.79–0.99) 0.044 0.89 (0.79–0.99) 0.046 0.94 (0.83–1.06) 0.294 
rs2736100 0.492 1.12 (1.01–1.24) 0.023 1.13 (1.02–1.24) 0.021 1.09 (0.99–1.22) 0.100 
rs7675998 0.210 1.03 (0.91–1.17) 0.621 1.03 (0.91–1.17) 0.599 1.05 (0.93–1.20) 0.459 
rs9420907 0.143 0.98 (0.85–1.13) 0.775 0.98 (0.85–1.13) 0.763 1.02 (0.88–1.18) 0.838 
rs6772228 0.048 1.15 (0.91–1.45) 0.242 1.15 (0.91–1.45) 0.245 1.09 (0.85–1.40) 0.477 
rs8105767 0.295 1.02 (0.91–1.13) 0.763 1.02 (0.91–1.14) 0.752 1.02 (0.92–1.15) 0.690 
rs11125529 0.140 1.02 (0.88–1.18) 0.773 1.02 (0.88–1.18) 0.787 1.00 (0.86–1.16) 0.975 
rs3027234 0.231 1.03 (0.91–1.16) 0.662 1.03 (0.91–1.15) 0.677 1.04 (0.92–1.18) 0.500 
GRS Quartiles Case: control       
1: ≤ 0.473 378: 370 1.00 (ref) 0.588 1.00 (ref) 0.585 1.00 (ref) 0.556 
2: > 0.473 - ≤ 0.567 337: 368 0.90 (0.73–1.10)  0.90 (0.73–1.10)  0.90 (0.73–1.12)  
3: > 0.567 - ≤ 0.662 385: 372 1.01 (0.83–1.24)  1.01 (0.83–1.24)  1.04 (0.84–1.28)  
4: > 0.662 383: 369 1.02 (0.83–1.24)  1.02 (0.83–1.25)  1.04 (0.84–1.29)  
Continuousb  1.02 (0.97–1.07) 0.492 1.02 (0.97–1.07) 0.483 1.03 (0.97–1.08) 0.325 
Short allele countsc        
2–6 434: 435 1.00 (ref) 0.137 1.00 (ref) 0.137 1.00 (ref) 0.117 
7 329: 369 0.89 (0.73–1.09)  0.89 (0.73–1.09)  0.88 (0.71–1.09)  
8 362: 315 1.15 (0.94–1.41)  1.15 (0.94–1.41)  1.16 (0.94–1.43)  
≥ 9 358: 360 1.00 (0.82–1.21)  1.00 (0.82–1.23)  1.02 (0.82–1.25)  
Continuous b  1.02 (0.98–1.07) 0.380 1.02 (0.98–1.07) 0.375 1.03 (0.98–1.07) 0.264 
Unadjusted modelAge- and sex-adjustedMultivariable-adjusteda
SNP IDMAFOR (95% CI)POR (95% CI)POR (95% CI)P
rs10936599 0.261 0.89 (0.79–0.99) 0.044 0.89 (0.79–0.99) 0.046 0.94 (0.83–1.06) 0.294 
rs2736100 0.492 1.12 (1.01–1.24) 0.023 1.13 (1.02–1.24) 0.021 1.09 (0.99–1.22) 0.100 
rs7675998 0.210 1.03 (0.91–1.17) 0.621 1.03 (0.91–1.17) 0.599 1.05 (0.93–1.20) 0.459 
rs9420907 0.143 0.98 (0.85–1.13) 0.775 0.98 (0.85–1.13) 0.763 1.02 (0.88–1.18) 0.838 
rs6772228 0.048 1.15 (0.91–1.45) 0.242 1.15 (0.91–1.45) 0.245 1.09 (0.85–1.40) 0.477 
rs8105767 0.295 1.02 (0.91–1.13) 0.763 1.02 (0.91–1.14) 0.752 1.02 (0.92–1.15) 0.690 
rs11125529 0.140 1.02 (0.88–1.18) 0.773 1.02 (0.88–1.18) 0.787 1.00 (0.86–1.16) 0.975 
rs3027234 0.231 1.03 (0.91–1.16) 0.662 1.03 (0.91–1.15) 0.677 1.04 (0.92–1.18) 0.500 
GRS Quartiles Case: control       
1: ≤ 0.473 378: 370 1.00 (ref) 0.588 1.00 (ref) 0.585 1.00 (ref) 0.556 
2: > 0.473 - ≤ 0.567 337: 368 0.90 (0.73–1.10)  0.90 (0.73–1.10)  0.90 (0.73–1.12)  
3: > 0.567 - ≤ 0.662 385: 372 1.01 (0.83–1.24)  1.01 (0.83–1.24)  1.04 (0.84–1.28)  
4: > 0.662 383: 369 1.02 (0.83–1.24)  1.02 (0.83–1.25)  1.04 (0.84–1.29)  
Continuousb  1.02 (0.97–1.07) 0.492 1.02 (0.97–1.07) 0.483 1.03 (0.97–1.08) 0.325 
Short allele countsc        
2–6 434: 435 1.00 (ref) 0.137 1.00 (ref) 0.137 1.00 (ref) 0.117 
7 329: 369 0.89 (0.73–1.09)  0.89 (0.73–1.09)  0.88 (0.71–1.09)  
8 362: 315 1.15 (0.94–1.41)  1.15 (0.94–1.41)  1.16 (0.94–1.43)  
≥ 9 358: 360 1.00 (0.82–1.21)  1.00 (0.82–1.23)  1.02 (0.82–1.25)  
Continuous b  1.02 (0.98–1.07) 0.380 1.02 (0.98–1.07) 0.375 1.03 (0.98–1.07) 0.264 

Abbreviation: MAF, minor allele frequency (among controls).

aAdjusted for age (continuous), sex, self-reported personal history of diabetes (yes, no), smoking history (never, former, current), and usual adult body mass index (continuous).

bCalculated as per 0.10 increase in kilobase pair of telomere length or per 1 short TL allele.

dAllele counts were categorized on the basis of distribution among controls. Lower “short allele count” values predict longer telomere length (3).

View Large
Table 2B.

Associations of telomere-related SNP and short telomere length allele counts with pancreatic cancer risk: Dominant model (cases: n = 1,500, controls: n = 1,499)

Long-allele genotypeaShort-allele genotypesbUnadjusted modelAge- and sex-adjustedMultivariable-adjustedc
SNP IDCase: controlCase: controlOR (95% CI)POR (95% CI)POR (95% CI)P
rs10936599 872: 826 627: 670 0.88 (0.76–1.02) 0.097 0.89 (0.77–1.02) 0.101 0.95 (0.81–1.11) 0.507 
rs2736100 352: 385 1136: 1097 1.14 (0.96–1.35) 0.126 1.14 (0.97–1.35) 0.121 1.12 (0.94–1.34) 0.196 
rs7675998 927: 931 570: 563 1.02 (0.88–1.18) 0.835 1.02 (0.88–1.18) 0.813 1.03 (0.88–1.20) 0.718 
rs9420907 35: 35 1465: 1461 1.00 (0.62–1.61) 0.991 1.00 (0.62–1.61) 0.999 0.98 (0.60–1.63) 0.953 
rs6772228 1,338: 1,352 161: 144 1.14 (0.90–1.44) 0.288 1.14 (0.90–1.44) 0.290 1.08 (0.84–1.39) 0.541 
rs8105767 129: 147 1369: 1348 1.15 (0.90, 1.48) 0.271 1.15 (0.90–1.48) 0.268 1.15 (0.89–1.50) 0.285 
rs11125529 35: 34 1464: 1462 1.00 (0.62–1.62) 0.991 1.00 (0.62–1.62) 0.994 0.93 (0.56–1.53) 0.770 
rs3027234 876: 894 618: 601 1.04 (0.90–1.21) 0.565 1.04 (0.90–1.21) 0.574 1.07 (0.92–1.25) 0.362 
Short allele countd  Case: control       
2–4  491: 506 1.00 (ref)  1.00 (ref)  1.00 (ref)  
5  546: 541 1.04 (0.88–1.24) 0.654 1.04 (0.88–1.24) 0.648 1.04 (0.86–1.24) 0.702 
>6  446: 432 1.06 (0.89–1.28) 0.503 1.07 (0.89–1.28) 0.494 1.11 (0.92–1.35) 0.280 
Continuouse   1.03 (0.96–1.10) 0.419 1.03 (0.96–1.10) 0.408 1.04 (0.97–1.12) 0.228 
Long-allele genotypeaShort-allele genotypesbUnadjusted modelAge- and sex-adjustedMultivariable-adjustedc
SNP IDCase: controlCase: controlOR (95% CI)POR (95% CI)POR (95% CI)P
rs10936599 872: 826 627: 670 0.88 (0.76–1.02) 0.097 0.89 (0.77–1.02) 0.101 0.95 (0.81–1.11) 0.507 
rs2736100 352: 385 1136: 1097 1.14 (0.96–1.35) 0.126 1.14 (0.97–1.35) 0.121 1.12 (0.94–1.34) 0.196 
rs7675998 927: 931 570: 563 1.02 (0.88–1.18) 0.835 1.02 (0.88–1.18) 0.813 1.03 (0.88–1.20) 0.718 
rs9420907 35: 35 1465: 1461 1.00 (0.62–1.61) 0.991 1.00 (0.62–1.61) 0.999 0.98 (0.60–1.63) 0.953 
rs6772228 1,338: 1,352 161: 144 1.14 (0.90–1.44) 0.288 1.14 (0.90–1.44) 0.290 1.08 (0.84–1.39) 0.541 
rs8105767 129: 147 1369: 1348 1.15 (0.90, 1.48) 0.271 1.15 (0.90–1.48) 0.268 1.15 (0.89–1.50) 0.285 
rs11125529 35: 34 1464: 1462 1.00 (0.62–1.62) 0.991 1.00 (0.62–1.62) 0.994 0.93 (0.56–1.53) 0.770 
rs3027234 876: 894 618: 601 1.04 (0.90–1.21) 0.565 1.04 (0.90–1.21) 0.574 1.07 (0.92–1.25) 0.362 
Short allele countd  Case: control       
2–4  491: 506 1.00 (ref)  1.00 (ref)  1.00 (ref)  
5  546: 541 1.04 (0.88–1.24) 0.654 1.04 (0.88–1.24) 0.648 1.04 (0.86–1.24) 0.702 
>6  446: 432 1.06 (0.89–1.28) 0.503 1.07 (0.89–1.28) 0.494 1.11 (0.92–1.35) 0.280 
Continuouse   1.03 (0.96–1.10) 0.419 1.03 (0.96–1.10) 0.408 1.04 (0.97–1.12) 0.228 

Abbreviation: MAF, minor allele frequency (among controls).

aReferent group for calculation of OR estimates.

bIndividuals with one or two copies of the short telomere length-associated allele were combined into one group.

cAdjusted for age (continuous), sex, self-reported personal history of diabetes (yes, no), smoking history (never, former, current), and usual adult body mass index (continuous).

dAllele counts were categorized on the basis of distribution among controls. A lower value of “short allele count” predicts longer telomere length (3).

ePer 1 short TL allele.

View Large

Epidemiologic studies of LTL and PDAC risk have yielded mixed results (2). This may be due to differences in the studied populations [e.g., heavy smokers (4) vs. population with < 15% smoking prevalence (5)], interlaboratory variation in LTL measurement, differences in the time between blood collection and cancer diagnosis, or a combination of these factors. To help clarify the conflicting reports, we used TL-related SNPs to genetically predict TL and examined association with PDAC. In age- and sex-adjusted models, short TL-associated alleles of rs10936599 and rs2736100 had opposite associations with PDAC risk. Results for GRS and short TL allele counts were null.

Our sample had sufficient statistical power to detect an association at the 0.05 significance level. On the basis of 1,500 cases and 1,499 controls, we had >80% power to detect an OR of 1.20 in the dominant model with three categories of short TL allele counts (Table 2B). Although validation in a consortium setting may be warranted, the findings indicate that genetically predicted TL is not associated with PDAC risk. LTL may represent an integrative biological marker of long-term exposure to risk factors of PDAC (e.g., smoking, obesity, and diabetes). Further delineation of the association between LTL and PDAC, using current industry standard methods (e.g., monochrome multiplex quantitative PCR) to measure TL in longitudinal studies, with multiple measures at biologically relevant stages in life may provide new insights.

No potential conflicts of interest were disclosed.

Conception and design: S.O. Antwi, W.R. Bamlet, L.A. Boardman, G.M. Petersen

Development of methodology: S. Antwi, G.M. Petersen

Acquisition of data (provided animals, acquired and managed patients, provided facilities, etc.): S.O. Antwi, L.A. Boardman, G.M. Petersen

Analysis and interpretation of data (e.g., statistical analysis, biostatistics, computational analysis): S.O. Antwi, W.R. Bamlet, B.T. Broderick, K.G. Chaffee, A. Oberg, L.A. Boardman, G.M. Petersen

Writing, review, and/or revision of the manuscript: S.O. Antwi, W.R. Bamlet, K.G. Chaffee, A. Oberg, A. Jatoi, L.A. Boardman, G.M. Petersen

Administrative, technical, or material support (i.e., reporting or organizing data, constructing databases): S.O. Antwi, W.R. Bamlet, B.T. Broderick

Study supervision: G.M. Petersen

Other: A. Jatoi

The authors thank the participants and dedicated staff of the Mayo Clinic Biospecimen Resource for Pancreas Research for their invaluable contributions to this study.

The study was supported by funding from the National Cancer Institute (P50CA102701 to G.M. Petersen, 5R25CA092049 to G.M. Petersen, and CA204013 to L.A Boardman), and a pilot grant from the Mayo Clinic Cancer Center (P30CA15083 to L.A Boardman and J. Jatoi).

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©2017 American Association for Cancer Research.
2017
American Association for Cancer Research.

Supplementary data

Supplementary Table 1

Characteristics of study participants

- docx file